Biomedical subjects

Pinar Yurdakul

Publications and source records attributed to Pinar Yurdakul.

5 recordsLinked to original sources

PubMed2006

[Isolation and identification of Burkholderia cepacia complex from cystic fibrosis patients].

In this study, sputum samples collected from cystic fibrosis patients with preliminary diagnosis of pulmonary infection were evaluated for the presence of bacteria belonging to Burkholderia cepacia complex by commercial phenotypic systems and recA polymerase chain reaction (PCR). A total of 85 patients ages between 5-30 years (mean age: 12.8 years) were included to the study with female/male ratio of 44/41. The mostly isolated bacteria from 85 sputum samples were found as Staphylococcus aureus (55.3%), Pseudomonas aeruginosa (48.2%) and Haemophilus influenzae (15.3%), whereas B. cepacia complex was phenotypically identified from two (2.3%) out of the samples. However only one was confirmed by PCR and typed as Burkholderia multivorans by restriction fragment lenght polymorphism method. This study emphasizes the importance of molecular methods as confirmatory tests for accurate identification of B. cepacia complex.

Adolescent↗

PubMed2005

[Immunopathogenesis of Leishmania infections].

Leishmaniasis represents a complex of diseases with a clinical and epidemiological diversity. Leishmaniasis remains a severe public health problem and its burden is increasing. The disease is caused by a parasite belonging to the genus Leishmania. Approximately 350 billion people in 88 different countries are thought to be infected with Leishmania spp. Clinical forms of leishmaniasis are particularly diverse representing different diseases: visceral (VL), cutaneous (CL), diffuse cutaneous (DCL) and muco-cutaneous (MCL) leishmaniasis. Being the most important determinant not only cellular immunity plays the essential role in the control of leishmaniasis, but the virulence, tropism and pathogenicity that is modulated by environmental and genetic factors of their mammalian hosts and sandfly vectors, are the key interactions. These eukaryotic pathogens have evolved with the vertebrate immune system and typically produce long lasting chronic infections. A critical step in their host interaction is the evasion of innate immune defenses. The ability to avoid attack by humoral effector mechanisms, such as complement lysis, and to resist killing by lysosomal enzymes and toxic metabolytes is of particular importance. They do so by remodelling the phagosomal compartments in which they reside and by interfering with signalling pathways that lead to cellular activation. In addition they modify the antigen presenting and immunoregulatory functions of dendritic cells, a process that fascilitates their evasion of both innate and adaptive immunity. Experimental animal studies revealed that these modifications and interference mechanisms led to two different pathogenesis schemes. For CL, the polarization of Th2/Th1 cells is responsible for the progression of the disease which than leads to the chronic-persistant state. The Th2/Th1 paradigm does not apply for visceral leishmaniasis. Immunosupression rather than polarization is responsible for the systemic and progressive outcome of the disease in VL. Based on experience with animal models and humans, new vaccine and novel immunotherapy strategies especially for the locations where the disease is endemic, hold promise for the near future. In this review article the immunopathogenesis of leishmaniasis has been discussed under the light of recent literature.

Animals↗

PubMed2004

Some fused heterocyclic compounds as eukaryotic topoisomerase II inhibitors.

Our previously synthesized 37 compounds, which are 2,5,6-substituted benzoxazole, benzimidazole, benzothiazole, and oxazolo(4,5-b)pyridine derivatives, were tested for their eukaryotic DNA topoisomerase II inhibitory activity in cell free system and 28 were found to inhibit the topoisomerase II at an initial concentration of 100 microg/ml. After further testing at a lower range of concentrations, 12 derivatives, which were considered as positive topoisomerase inhibitors, exhibited IC50 values between 11.4 and 46.8 microM. Etoposide was used as the standard reference drug to compare the inhibitor activity. Among these compounds, 2-phenoxymethylbenzothiazole (3f), 6-nitro-2-(2-methoxyphenyl)benzoxazole (1a), 5-methylcarboxylate-2-phenylthiomethylbenzimidazole (3c), and 6-methyl-2-(2-nitrophenyl)benzoxazole (1c) were found to be more active than the reference drug etoposide. Present results point out that, besides the very well-known bi- and ter-benzimidazoles, compounds with single bicycle fused ring systems in their structure such as benzimidazole, benzoxazole, benzothiazole, and/or oxazolopyridine derivatives also exhibit significant topoisomerase II inhibitory activity.

Animals↗

PubMed2003

Comparison of two methods and three end points in determination of in vitro activity of micafungin against Aspergillus spp.

We investigated the in vitro activity of micafungin against clinical Aspergillus isolates (n = 37) (Aspergillusfumigatus [n = 21], Aspergillusflavus [n = 14], and Aspergillus niger [n = 2]) by using NCCLS M38A microdilution and an investigational disk diffusion assay. Microdilution assay results were evaluated by using the end points of a MIC-2 (measured in micrograms per milliliter) and minimum effective concentration (MEC, measured in micrograms per milliliter; the lowest concentration of micafungin that produces short and aberrant hyphal branchings microscopically). Disk diffusion results were interpreted by measuring the zone(s) of inhibition (ZOI, measured in millimeters). Micafungin proved to be similarly active against all Aspergillus species tested. At 24 h, MIC-2s and MECs were identical. At 48 h, however, MIC-2s increased unpredictably, leading to the loss of a consistent correlation between the two end points. MECs and ZOI remained consistent and correlated at both reading times, suggesting their use as relevant end points in susceptibility testing of micafungin against Aspergillus: All Aspergillus isolates yielded intrazonal growth on disk diffusion agar plates. The intrazonal colonies contained short, aberrant hyphal branchings microscopically. The in vivo significance of these findings remains to be further investigated.

Antifungal Agents↗

PubMed2002

[Ecological factors for host tissue colonization].

The first stage of microbial infection is colonization; the establishment of the pathogen at the appropriate portal of the entry. Organisms that have the ability to colonize host tissues, have usually developed tissue adherence mechanisms and some ability to overcome or withstand the constant pressure of host defense mechanisms. There are namely 3 adaptations that are important for bacteria to colonize human hosts: Coaggregation, osmo-adaptation, acid tolerance and resistance. In this review article, these adaptation mechanisms have been discussed under the light of literature.

Adaptation, Physiological↗